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Twenty patients with mild, untreated arterial hypertension had ambulatory blood pressure recordings and a digitized echocardiographic study of the left ventricle with measurement of its mass (LVM) and of relaxation parameters. A significant correlation was found between LVM and ambulatory systolic pressure during daytime (r = 0.64; p less than 0.01; n = 20) and during 24 hours (r = 0.79; p less than 0.001; n = 16). One of the relaxation parameters studied, the time taken to reach maximal speed of left ventricular enlargement, was closely related to the diurnal diastolic blood pressure (r = 0.58; p less than 0.01; n = 20), whereas in this population with mild arterial blood pressure none of the parameters was related to the amount of increase of LVM. One may therefore consider the abnormalities of left ventricular relaxation as likely to appear at an early stage of arterial hypertension; their discovery may antedate that of LVM and confirm that the hypertensive disease is real. However, the methodological problems encountered with type of exploration ought to be stressed: left ventricular relaxation is a multifactorial phenomenon, and its echocardiographic approach is subject to many hazards.

Effects of Verapamil, 120 mg t.i.d. in twenty-one hypertensive patients were assessed at rest and during dynamic exercise. The selection criterion was a diastolic blood pressure (DBP) found, at least 3 times, between 95 and 115 mmHg, not responding to placebo therapy. After 30 days of treatment with Verapamil, the resting systolic blood pressure (SBP) and DBP respectively decreased from 151.8 to 137.5 mmHg (p less than 0.001) and from 103.2 to 89.8 mmHg (p less than 0.001). The blood pressure (BP) and heart rate (HR) responses to dynamic exercise were also significantly blunted and the BP profile on effort was normalized in about half of the cases. Finally, the automatic recording of BP by a non invasive device showed a fall in the mean blood pressure (MBP) from 100.6 to 90.8 mmHg (p less than 0.001). The best results were obtained in patients with lower pretreatment plasma renin activity index and higher DBP or MBP automatically measured. The degree of response was not significantly related to age nor to plasma homovanillic acid level, which, however, significantly rose in all patients following therapy. This increase in sympathetic tone suggests a vasodilatory effect of Verapamil. The tolerance was good in all patients but four, whose electrocardiogram showed some alteration of atrio-ventricular conduction.

The cerebral blood flow is maintained at a constant level in spite of blood pressure variations, because of a very performing auto-regulation phenomenon: vasoconstriction in case of elevated blood pressure, vasodilatation in case of blood pressure drop. The upper limit of the mean blood pressure beyond which nothing can prevent the cerebral blood flow from increasing, ranges between 150 and 170 mmHg. The lower limit, from which the dilatation of the cerebral blood vessels is not able to prevent the decreased cerebral blood flow, has been set between 50 and 70 mmHg. The auto-regulation of the cerebral blood flow is influenced by numerous factors: hypercapnia, hypoxia and ischemia complete inhibit it, making the cerebral blood flow directly related to the blood pressure; the sympathetic stimulation shifts the entire curve toward the right, because of the constriction of the pia-mater arteries, followed with a reactional vasodilatation of the small cerebral vessels. In the course of chronic arterial hypertension, the same shift of the auto-regulation curve toward high pressures is observed, related to structural alterations of the vascular wall; this make them more prone to constriction than dilatation: when these alterations are reversible, antihypertensive treatment may sometimes bring the auto-regulation curve in its initial position.

The authors have compared the anti-arrhythmic activity and tolerance of disopyramide and amiodarone in the treatment of ventricular extrasystoles (VES) by using two quantitative methods of assessment. The stability of the rhythmic disorder was confirmed by two control Holter recordings in 20 patients without treatment, 16 of whom were bearers of an organic cardiopathy. The ventricular extrasystole was greater than 90 VES/hour in 18 patients. After the first control, Holter recording, each patient was treated successively with 400 mg of disopyramide/day in 4 doses for average period of 31 days, then a second Holter control recording without treatment, then 600 mg/day of amiodarone for 8 days followed by a maintenance dose varying from 200 to 400 mg/day: this second period of treatment lasted for an average of 38 days. The reduction of the number of VES was greater than 65 percent (SAMI criterion) in 2 of the 20 patients treated with disopyramide and in 13 of the 20 patients treated with amiodarone. Using the method of variance analysis, disopyramide was found to be efficacious in 5 cases out of 20 and amiodarone in 15 cases out of 20. Both methods indicate that the greater efficacy of amiodarone is statistically significant (p less than 0.01). All of those who did not respond to amiodarone were also non-responders to disopyramide.

Twenty-one patients with mild or moderate hypertension were randomised to receive either Atenolol 100 mg (N = 10) or Pindolol 15 mg (N = 11) in a once daily dosage over a two month period. The effects of these two betablockers on the blood pressure and plasma lipid profile were studied. Special attention was paid to the methodology: obese patients (30% over theoretical weight derived from the Lorenz formula) and those with pre-treatment triglyceride levels higher than 1.82 mmol/l were excluded because of the well documented biological instability of such patients. The selected patients were given placebo for two weeks. At the end of the placebo period those subjects whose body weight, total cholesterol, apolipoproteins or triglycerides had varied by more than 10%, 15% and 30% respectively, were also excluded from the study. At the end of the 60 days active treatment period, a comparable fall in the blood pressure was observed in both groups and there was no significant difference in the biological parameters as compared with pre-treatment values. In addition, the cardiovascular risk, evaluated by the B/A1 apolipoprotein ratio, increased in only one patient in the group receiving Atenolol and one patient receiving Pindolol.

The authors report the case of a 41-year-old man suffering from primary hyperaldosteronism due to bilateral adrenal hyperplasia, predominantly on the left. This condition is somewhat less common than Conn's adenoma and differs distinctly on the basis of a very poor response to surgical treatment. It can generally be diagnosed by non-invasive techniques, the most reliable of which are the postural test and adrenal isotope scan under inhibition with dexamethasone. These methods are nevertheless not always valuable in the presence of certain forms of hyperplasia which are less distinct from an anatomical standpoint, and must then be complemented by adrenal phlebography and estimation of aldosterone in adrenal venous blood or, if this proves impossible, in the inferior vena cava and renal veins.

We studied the simultaneous effects of nifedipine on the pulmonary circulation and blood gases in 12 patients with pulmonary hypertension secondary to obstructive chronic bronchitis. Measurements were carried out at rest and during stress, initially then one hour after administration of 20 mg of nifedipine sublingually. They were repeated in a similar fashion after a 6-month treatment with 60 mg/day (group II) (30 mg/day in case of intolerance) (group I). The results of the immediate effect of nifedipine are in favor of a passive pulmonary vasodilatation secondary to the systemic vasodilatation. After six months of treatment, the pulmonary vasodilatation persists, but is associated with a decreased motor pressure indicating a more specific and more active pulmonary vasodilating effect of long-term nifedipine, especially during stress; this results in the improvement of the performance of the right ventricle without harmful effect on the blood gases. However, these results should be interpreted with caution on account of the small number of patients, the large interindividual variations and the absence of a reference population.

Hypertensive left ventricular hypertrophy can easily be diagnosed by echocardiography. It occurs in 30-50 per cent of hypertensive patients and has recently been shown to be a potent and independent predictor of morbidity and mortality, increasing the risk of sudden death, arrhythmia and severe coronary events. The condition usually presents as concentric left ventricular hypertrophy with symmetrically or asymmetrically thickened ventricular walls, but it may also be found with a dilated cavity. Its presence is a definite indication for active medical treatment. Guidelines for the choice of a particular antihypertensive drug are not yet available. Regression of the hypertrophy seems to be a rational goal of the treatment, but the beneficial effects of such a regression on left ventricular relaxation need further evaluation.

The efficacy of orally administered propafenone in the prevention of paroxysmal supraventricular dysrhythmias (atrial fibrillation, atrial tachysystole, reciprocal tachycardia) resistant to Vaughan-Williams class Ia drugs was investigated in 10 patients. Propafenone controlled dysrhythmia very well in 4 out of the ten patients, and satisfactorily in another one at a dosage ranging from 450 to 900 mg/day in 3 or 4 divided doses; this result was documented using continuous 24 hr. Holter ECG monitoring. Among the 5 clinical failures, 1 patient had atrial fibrillation primarily at night, and another poorly tolerated this agent which led to interrupt therapy.

Two case-reports of thrombopenias induced by pentosane polysulfate (PSP) are reported. PSP may play a direct role in the genesis of the thrombopenia appearing between the 5th and 15th day of treatment, or a sensitizing role where the thrombopenia occurs quite rapidly following heparin treatment. The clinical complications are haematomas, arterial or venous thromboses and haemorrhages. The platelet aggregation test is always positive in the presence of PSP. The immunological origin is probable. Monitoring of the platelet count is recommanded with this treatment.